Kathryn Lawson, Ph.D.

Associate Professor
Glendale, AZ

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Associate Professor

Glendale, AZ

Arizona College of Osteopathic Medicine
Arizona College of Optometry
College of Dental Medicine-Arizona
College of Graduate Studies - AZ
College of Health Sciences - AZ
College of Veterinary Medicine

Biochemistry and Molecular Genetics

Dental Medicine
Entry into Practice Doctor of Nurse Anesthesia Practice
Post Master's Doctor of Nurse Anesthesia Practice (D.N.A.P.)
Nurse Anesthesia Practice (M.S.)
Osteopathic Medicine
Physician Assistant Studies
Podiatric Medicine
Veterinary Medicine

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University of Arizona | 1998 | Ph.D.
University of Arizona | 1992 | B.S.


My laboratory uses genetically-modified human cell lines to study the way changes in cell adhesion proteins can contribute to tumor development.  We are specifically interested in the role of P-cadherin, a molecule located on the sides of cells that helps hold cells together to form tissues, and N-cadherin, which becomes abnormally expressed in epithelial cancers.   Current research efforts are focused on three areas in which cadherin expression may alter tumor development:

  1.  P-cadherin-dependent tumor progression in non-small cell lung cancer. Clinical studies have suggested that P-cadherin decreases overall survival in patients with non-small cell lung cancer tumors that have abnormally high levels of P-cadherin expression.  We are using genetically-modified lung cancer cell lines to examine the mechanisms by which P-cadherin may promote tumor development and aggressiveness.
  2. P-cadherin-dependent chemoresistance in Oral Squamous Cell Carcinoma. We have found that increased levels of P-cadherin can cause oral cells to exhibit either greater resistance or greater sensitivity to different classes of chemotheraputic drugs that are used to treat oral cancer.  We are currently using a proteomics (protein-based) approach to define the P-cadherin-driven signaling networks that play an important role in cell death vs. cell survival in cells treated with these agents.
  3. Metabolic consequences of N-cadherin in oral squamous cell carcinoma. We are using both an oral precancer and oral squamous carcinoma model system to evaluate the effects of N-cadherin on metabolic signaling, including stimulation the Warburg effect to increase both glucose utilization and anaerobic glycolysis.


1. Lysne, D, Johns J, Walker, A, Ecker R, Fowler, C, & Lawson KR.  "P-cadherin potentiates ligand-dependent EGFR and IGF-1R signaling in dysplastic and malignant oral keratinocytes". Oncology Rep. (2014) 32(6): 2541-2548.

2. Walker, A, Frei, R, and Lawson K.  "The cytoplasmic domain of N-cadherin modulates MMP-9 induction in oral squamous carcinoma cells". Int J. Oncology. (2014) 45(4):1699- 1706.

3. Maeda, M., Johnson, E., Mandal, S.H., Lawson, K. R., Keim, S. A., Svoboda, R. A., Caplan, S., Wahl, J. K., Wheelock, M. J., and Johnson, K.R. “Expression of inappropriate cadherins by epithelial tumor cells promotes endocytosis and degradation of E-cadherin via competition for p120ctn.." Oncogene. (2006) 25(33):4595-4604.

4. Lawson K, Larentowicz L, Artim S, Hayes CS, Gilmour SK. “A novel protein kinase CK2 substrate indicates CK2 is not directly stimulated by polyamines in vivo.” Biochemistry. (2006) (5):1499-510.

5. Lawson, K., Larentowicz L, Laury-Kleintop, L., Gilmour, S.K. “B23 is a downstream target of polyamine-modulated CK2.” Mol Cell Biochem. (2005) 274(1-2):103-14.



American Association For Cancer Research (1996 - present)

American Society for Biochemistry and Moleculear Biology (2018-present)